Diversity of channels involved in Ca(2+) activation of K(+) channels during the prolonged AHP in guinea-pig sympathetic neurons (original) (raw)
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Autonomic Neuroscience, 2006
Ca 2+ -activated K + channels play an important role in the control of neuronal excitability via the generation of the afterhyperpolarization. While both small and large conductance Ca 2+ -activated K + channels underlie afterhyperpolarizations in different neuron types, the role of intermediate conductance Ca 2+ -activated K + channels (IK Ca ) in the generation of afterhyperpolarizations remains unclear. The effects of blockade of IK Ca on guinea pig coeliac and ileal myenteric neurons were studied using single microelectrode current and voltage clamp. In coeliac neurons, TRAM-39, a selective blocker of IK Ca , depressed the amplitude of the prolonged conductance underlying the slow afterhyperpolarization, (gKCa2) by 57%. In contrast, the conductance underlying the prolonged afterhyperpolarization in AH-type myenteric neurons was unaffected by TRAM-39, although it has been suggested that this AHP is mediated by IK Ca . In both types of neurons, TRAM-39 did not alter the resting cell properties or the properties of the action potential. TRAM-39 had no effect on the amplitude of the fast component of the afterhyperpolarization present in sympathetic LAH neurons. The results of this study suggest that in sympathetic LAH neurons, activation of IK Ca underlies at least part of the prolonged afterhyperpolarization while the nature of the channel underlying the AHP in enteric neurons remains unclear. D
Electrophysiological roles of L-type channels in different classes of guinea pig sympathetic neuron
Journal of neurophysiology, 1999
The electrophysiological consequences of blocking Ca(2+) entry through L-type Ca(2+) channels have been examined in phasic (Ph), tonic (T), and long-afterhyperpolarizing (LAH) neurons of intact guinea pig sympathetic ganglia isolated in vitro. Block of Ca(2+) entry with Co(2+) or Cd(2+) depolarized T and LAH neurons, reduced action potential (AP) amplitude in Ph and LAH neurons, and increased AP half-width in Ph neurons. The afterhyperpolarization (AHP) and underlying Ca(2+)-dependent K(+) conductances (gKCa1 and gKCa2) were reduced markedly in all classes. Addition of 10 microM nifedipine increased input resistance in LAH neurons, raised AP threshold in Ph and LAH neurons, and caused a small increase in AP half-width in Ph neurons. AHP amplitude and the amplitude and decay time constant of gKCa1 were reduced by nifedipine in all classes; the slower conductance, gKCa2, which underlies the prolonged AHP in LAH neurons, was reduced by 40%. Surprisingly, AHP half-width was lengthened b...
The Journal of physiology, 1995
1. A focal extracellular suction electrode was used to investigate the contributions of K+ and Ca2+ currents to the nerve impulse recorded from sympathetic nerve terminals innervating the guinea-pig vas deferens in vitro. 2. Perfusing the electrode with Cd2+ (0.1-0.5 mM) had little effect on the configuration of the nerve impulse. 3. Perfusing the electrode with Ba2+ (1-3 mM) caused the appearance of a second negative-going component of the nerve impulse. Local application of Cd2+ (0.1 mM) had little affect on this component of the nerve impulse. 4. Perfusing the electrode with 4-aminopyridine (4-AP) and/or tetraethylammonium (TEA) caused the appearance of a second negative-going component of the nerve impulse. This component has been termed the late negative-going component (LNC). 5. The LNC produced by local application of 1 mM 4-AP and 10 mM TEA was not changed when the solution perfusing the electrode contained no added Ca2+, 10 mM Ca2+ or omega-conotoxin GVIA (0.1 microM). Perf...
Two distinct Ca-dependent K currents in bullfrog sympathetic ganglion cells
Proceedings of the National Academy of Sciences
Healthy bullfrog sympathetic ganglion cells often show a two-component afterhyperpolarization (AHP). Both components can be reduced or abolished by adding Ca-channel blockers or by removing external Ca. Application of a single electrode "hybrid clamp"--i.e., switching from current- to voltage-clamp at the peak of the AHP, reveals that the slow AHP component is generated by a small, slow, monotonically decaying outward current, which we call IAHP. IAHP is blocked by Ca-removal or by apamin and is a pure K current. It is slightly sensitive to muscarine and to tetraethylammonium ion but is much less so than muscarine-sensitive (IM) and fast Ca-dependent (IC) K currents. It also can be recorded in dual-electrode voltage-clamp experiments, where it is seen as a slow, small component of the outward tail current that follows brief depolarizations to 0 mV or beyond. IC is seen as an early, fast, large component of the same tail current. Both components are blocked by Ca removal, b...
Journal of neurophysiology, 1999
BK channel activation by brief depolarizations requires Ca2+ influx through L- and Q-type Ca2+ channels in rat chromaffin cells. Ca2+- and voltage-dependent BK-type K+ channels contribute to action potential repolarization in rat adrenal chromaffin cells. Here we characterize the Ca2+ currents expressed in these cells and identify the Ca2+ channel subtypes that gate the activation of BK channels during Ca2+ influx. Selective Ca2+ channel antagonists indicate the presence of at least four types of high-voltage-gated Ca2+ channels: L-, N-, P, and Q type. Mean amplitudes of the L-, N-, P-, and Q-type Ca2+ currents were 33, 21, 12, and 24% of the total Ca2+ current, respectively. Five-millisecond Ca2+ influx steps to 0 mV were employed to assay the contribution of Ca2+ influx through these Ca2+ channels to the activation of BK current. Blockade of L-type Ca2+ channels by 5 microM nifedipine or Q-type Ca2+ channels by 2 microM Aga IVA reduced BK current activation by 77 and 42%, respecti...
Proceedings of the National Academy of Sciences, 1985
The long-lasting after-hyperpolarization(s) (AHP) that follows the action potential in rat myotubes differentiated in culture is due to Ca2+-activated K+ channels. These channels have the property to be specifically blocked by the bee venom toxin apamin at low concentrations. Apamin has been used in this work to analyze, by electrophysiological and biochemical techniques, the role of innervation in expression of these important channels. The main results are as follows: (i) Long-lasting AHP that follows the action potential in rat myotubes in culture disappears when myotubes are cocultured with nerve cells from the spinal cord under the conditions of in vitro innervation. (ii) Extensor digitorum longus muscles from adult rats have action potentials that are not followed by AHP but AHP are systematically recorded after muscle denervation and they are blocked by apamin. (iii) Specific 1251-labeled apamin binding is undetectable in innervated muscle fibers but it becomes detectable 2-4 days after muscle denervation to be maximal 10 days after denervation. (iv) Apamin receptors detected with 1251-labeled apamin are present at fetal stages with biochemical characteristics identical to those found in myotubes in culture. The receptor number decreases as maturation proceeds and 1251-labeled apamin receptors completely disappear after the first week of postnatal life, in parallel with the disappearance of multi-innervation. All these results taken together strongly suggest an all-or-none effect of innervation on the expression of apamin-sensitive Ca2+-activated K+ channels. Ca2+-activated K+ channels are present in a variety of excitable and nonexcitable tissues (1, 2). These channels appear to serve a variety of physiological functions. Some of them are responsible for long-lasting after-hyperpolarizations (AHP) that follow action potentials (3-5), others play an essential role in K+ secretion by exocrine acinar cells (6, 7), others are involved in the electrical response to glucose, which controls insulin secretion by pancreatic 8 cells (8), others probably play a safety role to prevent the invasion of Ca2+ in cells that have voltage-dependent Ca2+ channels (9, 10), etc. Ca2+-activated K+ channels have also been impli
Role of Ca 2+Activated K + Channels on Adrenergic Responses of Human Saphenous Vein
American Journal of Hypertension, 2007
We studied the participation of K+ channels on the adrenergic responses in human saphenous veins as well as the intervention of dihydropyridine-sensitive Ca2+ channels on modulation of adrenergic responses by K+ channels blockade.Saphenous vein rings were obtained from 40 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension.Iberiotoxin (10−7 mol/L), an inhibitor of large conductance Ca2+-activated K+ channels, and charybdotoxin (10−7 mol/L), an inhibitor of both large and intermediate conductance Ca2+-activated K+ channels, enhanced the contractions elicited by electrical field stimulation and produced a leftward shift of the concentration–response curve to norepinephrine. In contrast, the inhibitor of small conductance Ca2+-activated K+ channels apamin (10−6 mol/L) did not modify the contractile response to electrical field stimulation or norepinephrine. In the presence of the dihydropyridine Ca2+-channel blocker nifedipine (10−6 mol/L), iberiotoxin and charybdotoxin failed to enhance the contractile responses to electrical field stimulation and norepinephrine.The results suggest that large conductance Ca2+-activated K+ channels are activated by stimulation with norepinephrine to counteract the adrenergic-induced contractions of human saphenous vein. Thus, inhibition of these channels increases significantly the contraction, an effect that appears to be mediated by an increase in Ca2+ entry through L-type voltage-dependent Ca2+ channels.